Hormonal control of apoptosis: the rat prostate gland as a model system

Methods Cell Biol. 1995;46:369-85. doi: 10.1016/s0091-679x(08)61936-6.


Because of the large proportion of cells that undergoes apoptosis in response to castration and because of the predictable time in which apoptosis occurs subsequent to castration of an adult male, the rat ventral prostate gland provides a superior model system in which to study the process of apoptosis in vivo. This model system has already proven to be one of the more fertile systems for the identification of specific gene products that have the potential to effect apoptosis. Unfortunately, this in vivo system has limited usefulness for the types of genetic manipulations required to prove the role of any given gene product in the onset and procession of apoptosis. Direct genetic manipulation of a living tissue remains a goal of molecular biology-based therapies, especially for peripheral tissues such as the prostate gland. Appropriate in vitro (cell culture) models in which to study androgen-regulated apoptosis of prostate cells are currently unavailable because prostate epithelial cells, once established in culture, are no longer dependent on androgenic steroids. In the future, genetic approaches involving gene targeting through transgenic mouse technology may provide the kind of information needed to evaluate the role of individual gene products in prostate cell apoptosis.

Publication types

  • Review

MeSH terms

  • Androgen Antagonists / pharmacology
  • Androgens / pharmacology*
  • Androgens / physiology
  • Animals
  • Apoptosis / drug effects*
  • Calcium Channel Blockers / pharmacology
  • DNA Damage
  • Dactinomycin / pharmacology
  • Gene Expression Regulation / drug effects
  • Male
  • Orchiectomy
  • Prostate / cytology
  • Prostate / drug effects*
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger / metabolism
  • Rats


  • Androgen Antagonists
  • Androgens
  • Calcium Channel Blockers
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Dactinomycin